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B activation and
inflammatory response in taurocholate-induced pancreatitis
Department of Medicine, Veterans Affairs Greater Los Angeles Healthcare System and the University of California, Los Angeles, Los Angeles, California 90073
Transcription factor nuclear
factor-
B (NF-B) is activated in cerulein pancreatitis and
mediates cytokine expression. The role of transcription factor
activation in other models of pancreatitis has not been established.
Here we report upregulation of NF-B and inflammatory molecules, and
their correlation with local pancreatic injury, in a model of severe
pancreatitis. Rats received intraductal infusion of taurocholate or
saline, and the pancreatic head and tail were analyzed separately.
NF-B and activator protein-1 (AP-1) activation were assessed by gel
shift assay, and mRNA expression of interleukin-6, tumor necrosis
factor-
, KC, monocyte chemoattractant protein-1, and inducible
nitric oxide synthase was assessed by semiquantitative RT-PCR.
Morphological damage and trypsin activation were much greater in the
pancreatic head than tail, in parallel with a stronger activation of
NF-B and cytokine mRNA. Saline infusion mildly affected these
parameters. AP-1 was strongly activated in both pancreatic segments
after either taurocholate or saline infusion. NF-B inhibition with
N-acetylcysteine ameliorated the local inflammatory
response. Correlation between localized NF-B activation, cytokine
upregulation, and tissue damage suggests a key role for NF-B in the
development of the inflammatory response of acute pancreatitis.
acute pancreatitis; nuclear factor-B; activator protein-1; cytokines; chemokines; inducible nitric oxide synthase
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